Key result
A 68-year-old man developed Takotsubo cardiomyopathy ten days after a mild COVID-19 infection, demonstrating that COVID-19 can trigger stress-induced cardiomyopathy.
Why the study?
Takotsubo cardiomyopathy is scarcely seen in COVID-19 patients, despite a wide range of reported cardiovascular manifestations.
Case Report (n=1)
COVID-19 can trigger Takotsubo cardiomyopathy, highlighting the need for clinical suspicion of stress-induced cardiomyopathy in COVID-19 patients presenting with new left ventricular dysfunction.
Answers are grounded in this paper and cite their sources.
TCM should be considered in COVID-19 with acute LV dysfunction; single case leaves association and incidence open.
Coronavirus disease 2019 (COVID-19) has a wide range of clinical manifestations, affecting multiple organ systems. Cardiovascular manifestations of COVID-19 that have been reported include arrhythmias, myocarditis, and an increased predisposition to acute myocardial infarction. Takotsubo cardiomyopathy (TCM), which is characterized by apical ballooning of the heart leading to acute left ventricular dysfunction, is scarcely seen in COVID-19 patients. We present a case of COVID-19-associated TCM in a 68-year-old man. A 68-year-old man with no significant past medical history presented with sudden-onset midsternal pressure-like chest pain at rest, associated with diaphoresis and shortness of breath. This occurred ten days after diagnosis of COVID-19 with mild symptoms, with no other recent physical or emotional stressors. At presentation, he was afebrile (98.5 °F), hypertensive (177/108 mmHg), tachycardic (HR 118 bpm), and saturating 100% on room air. Labs were significant for leukocytosis with 15.1 × 103 WBCs/mcL, elevated creatinine (1.46 g/dL), brain natriuretic peptide (BNP) of 156, troponin of 4 ng/mL that peaked at 16.28 ng/mL. The rapid COVID-19 test was positive. EKG showed anterolateral ST elevation and QTc interval of 446 ms. Echo showed severe hypokinesis of mid and apical segments and severely decreased left ventricular ejection fraction (LVEF)of <30%. Emergent left heart catheterization showed 75% mid left anterior descending coronary artery (LAD) stenosis and moderate right coronary artery (RCA) disease, while the ventriculogram showed a left ventricular ejection fraction of 35% with anteroapical and inferoapical akinesia suggestive of Takotsubo cardiomyopathy. The patient was placed on aspirin, ticagrelor, and atorvastatin, carvedilol, and lisinopril. EKG the next day showed a prolonged QTc of 526 ms with T-wave inversion and no ST elevations. The patient had no findings consistent with myocarditis or pheochromocytoma. He was discharged two days later. Within the next few weeks, his symptoms improved, and a follow-up echo confirmed normalization of left ventricular function. There has been an increased incidence of Takotsubo cardiomyopathy during the COVID-19 pandemic compared to the pre-pandemic period. There is only a slight female preponderance in COVID-19-induced TCM, possibly because males are predominantly affected by COVID-19. Our patient satisfied all four Mayo Clinic criteria required for the diagnosis of TCM. Pathophysiology of TCM in COVID-19 is linked with cytokine storm and consequent catecholamine surge. Most patients improve within succeeding weeks or months. Nonetheless, the case fatality rate is high 36.5%, which is significantly higher compared to TCM patients without COVID-19. COVID-19 has a multisystem involvement with various clinical presentations. New cardiomyopathy in COVID-19 patients should raise suspicion among clinicians regarding stress-induced cardiomyopathy.
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Noor et al. (2022) conducted a case report in Takotsubo Cardiomyopathy associated with COVID-19 (n=1). COVID-19 infection was evaluated. A 68-year-old man developed Takotsubo cardiomyopathy ten days after a mild COVID-19 infection, demonstrating that COVID-19 can trigger stress-induced cardiomyopathy.
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